 Physiologic homeostasis depends on normal fluid

and electrolyte balance, and is important in both

health promotion and treatment of disorders. Fluid
and electrolyte imbalances commonly accompany
illnesses. Severe imbalances may result to death
Some imbalances affect not only the acutely and
chronically ill but also clients with faulty diet or those
who take selected medication such as diuretics and
glucocorticoids preparation. Every nurse must
understand the process of fluid and electrolyte
balance identify client at risk for imbalances,
recognize early signs and symptoms of imbalances,
intervene as appropriate and evaluate the outcomes.
*Body Water
Principal body fluids ;solvent responsible for the body’s
structures and function.
Consists of 45-75% of the total body weight.
 NORMAL WATER
DISTRIBUTION/BALANCE
Body Fluids Function
 Facilitates transport of nutrients,
hormones, CHON and other
molecules into the cells.
 Aids in the removal of cellular
metabolic waste products.
 Provides the medium in which
cellular metabolism takes place.
 Regulates lubrication of musculo-
skeletal joints.
 Acts as a component all body
cavities ( pericardial fluid, pleural,
CSF)
 Fluid Compartments:
1. Intracellular Fluid (ICF)
– Includes all water
and electrolytes
inside the cells.
– 2/3 of the body
weight is contained
within cell
membranes
2. Extra cellular Fluid (ECF)
– Includes interstitial fluid,
intravascular and
Trancellular fluid
– Constitutes about 1/3 of
body water
Functions of ECF:
– Transports nutrients and
electrolytes to cell and
waste products for
excretion
– Regulates heat
– Lubricates and cushions
joints
– Hydrolyzes food for
digestive process
 NORMAL WATER BALANCE

Intake Output
Liquid 1,200-1,500 ml Urine 1,200 -1,500 ml
Water in food 700- 1,000 ml Feces 100-250 ml
Metabolism 200- 400 ml Insensible Loses:
Skin 350 -400 ml
Lungs 350- 400 ml
TOTAL 2,100 – 2,900 ml TOTAL 2,100 – 2,900 ml
Fluid Intake & Output
Routes of Gains and Losses
 CONTINUAL MOVEMENT OF FLUIDS
AND ELECTROLYTES
 Fluids move between
components to maintain
homeostasis
 Fluid Movement from Pressure
Changes-body fluid shifts
between the interstitial space
and the vascular space in the
capillary as a result of
differences in the hydrostatic
pressure and oncotic pressure
 Fluid Movement by Diffusion and Osmosis

 Diffusion- means by which substances such as

nutrients and wastes produces move between blood
and interstitial spaces.
 Osmolality – refers to the concentration of
solutes in 1 liter of solution
 OSMOSIS: diffusion of H2O across a selectively
permeable membrane from an area of lower solute
concentration to an area of higher solute
concentration.
 FACTORS RESPONSIBLE FOR NORMAL
REGULATION AND FLUID BALANCE
Regulator of fluids Balance:

 Thirst
– Hypothalamus- thirst
center of the brain
– Activated by an increase
in ECF Osmolality due to:

 Hypotension
 Polyuria

 Fluid volume depletion

 Hormones/ Hormonal
Influence
 Antidiuretic Hormone (ADH)-
stored in the posterior
pituitary gland; reduces
urinary output; returns fluids
to the body rather than
excreting them
 Aldosterone - secreted by
the adrenal cortex and
conserves the body’s sodium
by promoting potassium
excretion from the kidneys.
 Lymphatic system – It plays
an important role in returning
excess fluid and protein from
interstitial spaces to the
blood.
  RENIN-ANGIOTENSIN MECHANISM
 ATRIAL NATRIURETIC PEPTIDE
 Nervous System - when the ECF volume
increases, mechanoreceptors in the wall of
the atrium respond to atrial distention by
increasing cardiac stroke volume and
triggering a sympathetic response in the
kidney, stimulation of the of the renal
sympathetic nerves decreases renal
excretion of sodium by both increasing renin
release and through a direct effect in the
kidneys.
 Kidney – maintain fluid volume and the connection
of urine by filtrating the ECF through the glomeruli.
Reabsorbtion and excretion of ECF occurs in the
renal tubules.
 Fxns of the Kidneys
 Regulation of ECF volume and
osmolality by selective retention of
needes substances and excretion
fluids.
 Regulation of electrolytes level in the
ECF by selective retention of
substances and excretion of unneeded
substances
 Regulation of pH of the ECF by
retention of H+ ions
 REGULATION OF FLUID VOLUME

HYPERVOLEMIA HYPOVOLEMIA

inhibits stimulates

ADH Aldosterone Thirst Thirst ADH Aldosterone

INCREASED DECREASED
URINATION URINATION
of of
Dilute urine Concentrated urine

NORMAL FLUID VOLUME RESTORED

 FLUID IMBALANCES
I. Extra Cellular Fluid Volume Deficit
MILD: 1-2 L of H2O (2% body wt.)
Causes: MODERATE: 3-5 L of H2O (5%)
1. Lack of fluid intake SEVERE: 5-10 L of H2O (8%)
– 1,500 – 2,000 ml

RF:
– Hospitalized/bed bound
– People w/ dysphagia/ risk for aspiration
– Tube-fed patients who are not given adequate free water
– Pts. w/ decreased access to fluids
– Pts. w/ impaired thirst mechanism
 People w/ debilitating illnesses
 Older adults
2. Excessive Fluid Losses

– Vomiting, diarrhea, fever, hyperglycemia, suction,

fistula, burns, blood loss, diabetes insipidus,
diaphoresis, hyperthyroidism, excessive diuretics,
ileostomy, hyperventilation, Diuretic phase of ARF

Types of ECFVD
 Hyperosmolar (hypertonic): water loss is > electrolyte loss
 Hypotonic: electrolyte loss is > fluid loss
 Isotonic (iso-osmolar): water and electrolyte loss are equal
CLINICAL MANIFESTATIONS:
1. Loss of body wt.
– Most accurate indicator of fluid loss
– 1 L of sol’n=1 kg of body wt.

2. Changes in I &O
– U. O. of 400-500 ml/day- oliguria
– Thirst

3. Changes in V/S
– ↓ed BP
– Weak pulse
– ↓ed CVP, ↓ed PCWP
– Postural hypotension
– ↑ed PR
– Flat JV and prolonged peripheral venous filling time of more than 5 sec.
– Elev. Body temp
4. Manifestations of cellular dehydration
– dry mucus membrane of mouth and eyes
– cracked lips
– poor skin turgor
– muscle weakness
– cerebral sx (fluid shifting)
 FLUID VOLUME DEFICIT

•IS move to IV
•ADH & aldosterone is released
•Fluids reabsorbed in the ileum & colon
•Baroreceptors  SNS: increase HR &
Peripheral vasoconstriction
•Osmoreceptors: Thirst mechanism

DEHYDRATION

•Impaired temperature regulation

•Decrease ability to transport heat
•Decrease CSF
•Decrease Sodium
II. Intracellular Fluid Volume Deficit (ICFVD)
– Due to severe dehydration
RF:
- older clients; w/ acute water loss
s/sx:
- Thirst
– Oliguria
– Fever
– Confusion, coma, cerebral hemorrhage

 DIAGNOSTIC TEST FOR ECFVD/ICFVD:

Osmolality > 295 mOsm/L Na >145 mEq/l
BUN > 25 mg/dl Glucose >120 mg/dl
Hct > 55% Urine sp. Gr. > 1.030
III. Extra Cellular Fluid
Volume Excess
(ECFVE)
Fluid overload
2 types:
1. hypervolemia-↑ed fluids in
vascular system
2. third spacing-↑ed fluids in
interstitial space
 Etiology
 Simple overloading of fluids (too many
IVF)
 ↑ ADH and aldosterone
 ↓ kidney fxn
 CHF
 Liver Cirrhosis
 Venous disorder
 Excessive ingestion of fluids/ food with
Na
 MECHANISM OF EDEMA FORMATION
FLUID OVERLOAD
Increase hydrostatic
pressure in arterial end
of capillary

Increased peripheral
Vascular resistance
Fluid movement
into tissues

Increased left
Ventricular pressure

edema
Increased left atrial
pressure

Pulmonary edema
DECREASE PLASMA ALTERED LYMPHATIC TISSUE INJURY
& ALBUMIN FUNCTION

Decrease production Lymphatic obstruction Increase capillary

decreases absorption
of plasma CHON permeability
of interstitial fluid

Decrease Capillary Decrease transport Movement of plasma

Oncotic Pressure of capillary filtered
CHON in tissues
protein

Decrease
Increase tissue oncotic Increase tissue
Reabsorption pressure, which pulls
At venous end Oncotic pressure
fluid towards it

EDEMA EDEMA
EDEMA
 IMPAIRED RENAL FXN

↓ Na and H20 excretion

↑ Fluid Volume

Heart compensates by increasing

HR and Hypertrophy

If compensatory mechanism fails,

heart failure develops
  Clinical Manifestations:
> respiratory
> cardiovascular
> others
Edema
Anorexia/bloating
Wt. gain
Fluid shifting from IV/IS

DIAGNOSTICS:
Osmolality < 275 mOsm/L Na < 135 mEq/l
BUN < 8 mg/dl Urine sp. Gr. < 1.010
Hct < 45%
IV. Intracellular Fluid Vol. excess (ICFVE)- water intoxication;
cells are resistant to fluid shifts
Etiology:
– water excess- number of solutes is normal but there
is water excess
– solute deficiency=amt. of water is normal but ↓ed
solute
= most common cause: administration of excessive amts. Of
hypoosmolar IVF
= adults who
consume excessive amts. of tap H2O
w/o adequate nutrient intake
=SIADH
=people w/ psych. d/o → schizophrenia
with compulsive water consumption
V. Extracellular Fluid Volume Shifting – third spacing

2 types:
1. vascular fluid shifts to interstitial space (hypovolemia)
2. interstitial fluid shifts to vascular space (hypervolemia)
* third space= fluid that shifts into IS and remains there
= common sites:pleural cavity, peritoneal cavity, &
pericardial sac
Etiology:

 ↑ ed capillary permeability
 ↑ ed fluid reabsorption in venous end
 Decreased serum CHON levels
 Obstruction of venous end of capillary
 Non-functional lymphatic drainage system
Clinical Manifestations:
1. Fluid shifting from IV to IS
– Pallor, cold limbs, weak &rapid pulse,
hypotension, oliguria, ↑ ed skin turgor & ↓ ed level
of consciousness
– No changes in body wt. because fluid has not
been lost but redistributed
2.fluid returns to the IV space from IS – s/sx similar to
fluid overload
– bounding pulse, crackles, JVD, ↑ ed BP
 Types of Intravenous Fluids
Types of Intravenous Fluids:

 ISOTONIC – a solution that has the same osmotic pressure

externally as that found across a semi-permeable membrane
--0.9% NaCl, D5W, 5% Dextrose in 0.225% Saline and LRS

 HYPOTONIC –a solution that has a lower osmotic press than

that of the blood causing the cell to expand and swell.(They
contain lower concentration of salt/ solute than other solution)
--0.3 % NaCl, D in water, 0.45 % NaCl and distilled water.

 HYPERTONIC – a solution that has a higher osmotic pressure

than that of the blood causing the cell to shrink. ( It has higher
concentration of solutes.)
--D5LRS, Mannitol, 10% D in water, and 5% D in 0.45% NaCl
Cell appearance on different solutions

Blood cells in an
Hypotonic Fluid

Blood cells in an
Hypertonic Fluid
Electrolytes – these are chemical substances which
when dissolved dissociates into ions and passes
electrical potential.

Types:
 Cations – ions carrying positive charge
– Na
– K
– Ca
– Mg

 Anions – ions carrying negative

 CATIONS ANIONS
Na- 135-145 m Eq/L
HCO3- 22-26 mEq/L
K- 3.5 – 5.0 m Eq/L
Cl- 96-106 mEq/L
Ca- 4.5-5.5 mEq/L
PO4 – 1.2 -3.0 mEq/L
Mg -1.5 – 2.5 mEq/L
 A. Sodium Imbalances
 Derminant of serum osmolality
 Chloride is the anion that usually accompanies
Na
 Sodium balance is regulated by the interaction
among neural, hormonal, and vascular
mechanisms
 Renal glomerulus filters 1000 mEq of sodium/hr
and 99% is reabsorbed in the loop of Henle
 Prostaglandin
 FUNCTIONS
 Primary regulator of ECF volume
 Establishing electrochemical state
necessary for muscle contraction and
nerve impulse transmission
“WHERE SODIUM GOES WATER
FOLLOWS”
1. Hyponatremia –one of the most common electrolyte imbalance
Hypovolemic: Na loss > H2O loss
Euvolemic: TBW is mod. increased & total body Na is normal
Hypervolemic: Greater increased in TBW than in total Na
Redistributive: no change in TBW or total body Na.
RF:
 Excessive perspiration
 Altered thirst mech.
 w/o access to fluids
 rapid rehydration after excessive fluid loss
 altered percentage of total body water
 decreased intake of sodium: fruits, vegetables, oatmeal, rice, wheat, fresh
meat, chicken, fish (1 oz)
 excessive administration of diuretic and laxatives
 NGT irrigation with plain water
 Vomiting, drh
Clinical Manifestations: 125 mEq/L
 neurological manifestations
 Cardiovascular manifestations
– Tachycardia-
– Sympathetic responses – stimulation of
chemoreceptors in the aortic and carotid bodies
 Respiratory Manifestations
– Crackles in the lungs
– Tachypnea, dypnea, orthopnea, SOB
 GI Manifestations
– n/v, drh, abdominal cramping, hyperactive bowel
sounds
 Others:
– Dry skin, tongue & mucus membrane
 DX results:
 Na < 135 mEq/L
 Cl < 96 mEq/L
 Serum Osmolality <275 mOsm/kg
 Urine Osmolality <40 mOsm/kg
2. Hypernatremia - associated w/ water loss or sodium
gain

Types:
– Hypovolemic hypernatremia: TBW is greatly
decreased compared to Na

– Euvolemic hypernatremia: TBW is decrease

relative to normal total body Na

– Hypervolemic hypernatremia: TBW is increased

but Na gain is > H2O gain
Etiology/RF:
 Inadequate water intake in conjunction w/ decreased thirst
(hypodipsia)
 Lack of access to drinkable water
 Physical or chemical restraint
 Mental confusion
 NPO
 Excessive water loss & insufficient water replacement
 Increased Na+ intake: bread, cereals, chips, convenience food, fast foods
 IV administration of hypertonic saline or hypertonic tube
feedings
 Retention of Na+ occurs in heart, renal or liver dse.
 Cushing’s Syndrome
 Hyperaldosteronism
 Uncontrolled DM
Clinical Manifestations: 155 mEq/L

 Polyuria
 Anorexia, N/V, weakness, restlessness
 Early neurologic S/Sx
 Hypervolemic state
 Hypovolemic state
 Dysrhythmia
 Crackles, dysnea, pleural effusion
 Fever and increased thirst
 Dry skin and mucous membrane, tongue furrows
Effect of Sodium to cells
 B. Potassium Imbalances
 PISO
 Poorly stored in the body, daily K+ intake is necessary
 80 to 90% of K+ is excreted through the kidneys &
remainder is excreted in feces

Functions:
 Regulates ICF osmolality
 Promotes transmission and conduction of nerve impulses
 Muscle contraction
 Enzyme action for cellular metabolism and glycogen
storage in the liver
 acid-base balance
Alkalosis
– can cause hypokalemia
Acidosis
– can cause hyperkalemia
Substance that can alter K+ levels:
– Insulin
– Glucagon
– Adrenocortical hormones
 cortisol and aldosterone
 Stress

– Catecholamines & beta- adrenergic agonists

– Alpha-adrenergic agonists
– Epinephrine
– has alpha & beta – adrenergic properties
 1. Hypokalemia
- common, especially in elderly pop’n
Etiology and RF:
A. Inadequate K+ intake body does not conserve K+
– Debilitated, confused, restrained, lacking access to K+
sources, malnourished, anorexic, bulimic
– Potassium- restricted diets or some wt. reduction diets
( corn, potato, apple, blueberry, cranberry, coffee, cola,
gingerale, soda)
– Those receiving K+ free IV sol’ns
B. K+ excretion exceeds K+ intake
– Vomiting, drh, suctioning, intestinal fistulae,
ileostomy
– Osmotic diuresis that occurs with DKA
– Surgical clients
– Alcoholic clients
– Certain drugs (loop, osmotic, thiazide diuretics,
cathartics, steroids)
– Clients who are in the healing phase after a
severe tissue injury or burn
– Cushing’s syndrome
– Diuretic Phase of RF
– Hyperaldosteronism
 ↓ serum K

↓ K gradient

↑ resting membrane potential

↓ neuromuscular irritability
and excitability
Clinical Manifestations:
 GI Manifestations
– Slowed smooth muscle contraction
– Anorexia, abdominal distention, constipation
– Extreme smooth muscle slowing - vomiting ileus, urinary retention
 Slowed Skeletal Muscle Contraction- muscle weakness, Leg cramps,
fatigue, paresthesia, hyporeflexia, paralysis
 ECG-most reliable tool for identifying abnormalities in intracellular K+
level (peaked P wave, ST depressed & prolonged, Depressed or
inverted T wave, prominent U wave).
 ↓ ed myocardial contractility
 Pulmonary manifestations
 Progressive neurologic consequences of altered conduction –
dysphasia, confusion, depression, convulsions, areflexia, coma
 Polyuria, nocturia
 2. Hyperkalemia
Etiology and RF:
 Retention of K+ by the body because of ↓ ed or
inadequate urine output
 Release of K+ from the cells during the 1st 24 to 72 hours
after traumatic injury on burns, or from cell lysis or
acidosis
 Excessive infusion of IV solution that has K+ or excessive
oral intake of K+, especially in a person who has renal
dse
 Therapy w/ K+ sparing diuretics, use of K+ supplements,
ACE inhibitors
 Adrenal insufficiency or addison’s disease
 ↑ serum K

Altered resting membrane potential

Cell membrane becomes easily excitable

Increased depolarization or action potential

Repeated irritation of cell membrane

↑ Excitation threshold of membrane

Cells become less excitable

Weak, flaccid paralysis of muscles

Clinical Manifestations:

 N/V
 Diarrhea
 Impaired nerve & muscle function
 Severe neuromuscular weakness
 respiratory muscle paralysis
 ECG changes: (wide flat P wave, Depressed ST
segment, Narrow, peaked T wave)
 Impaired cardiac conduction (tachycardia,
hypotension, cardiac arrest, ventricular contractions)
Effect of Potassium on ECG
 C. Calcium Imbalances:
FUNCTIONS:

 catalyst (nerve impulses)

 stimulates muscle contraction
 normal cellular permeability
 blood coagulation
 absorption of Vitamin B12
 Bones and teeth
 99% of the body’s Ca# is in the bones & teeth
 1 % is in the tses. And IV space
3 types:
1. free/ ionized
2. Ca# bound to CHON
3. Complex

Vit. D - is needed to absorb Ca# from GIT

PTH
– regulates plasma levels of Ca# and PO4 by ↑ ing
resorption from bone and reabsorption from renal
tubule or the GIT
Calcitonin
– thyroid gland
– opposes action of PTH
– inhibits bone resorption
 1. Hypocalcemia
Etiology and RF:
 common in adult because of inadequate intake of Ca# and
Vit. D (GI dses – anorexia, liver dse., lactose intolerance,
alcoholism): oatmeal, hamburger, apples, bananas,
chicken
 decreased intake for several days (NPO), high CHON diet
 hypoparathyroidism
 people who don’t have exposure to the sun
 pancreatitis
 Open wounds
 Excess Na
 Overcorrection of Acidosis
 Multiple BT
 Certain drugs
– MgSO4, Colchicine, and neomycin
– Aspirin, anticonvulsants, and estrogen
– PO4prep’n
– Steroids
– Loop diuretic
– Antacids and laxatives
 ↓ Calcium

Partial depolarization of nerves and muscles

because of ↓ threshold potential

Smaller stimuli initiates the action potential

Clinical Manifestations:
 paresthesia
 ↓ ed CO
 ↑ ed peristalsis and drh
 Prolonged bleeding times and hemorrhage
 Bones become brittle and results in pathologic
fractures
 Facial Twitching (Chvostek’s sign)
 Carpopedal spasm (Trousseau’s sign)
 ECG changes: prolonged QT interval
 Severe: seizure, tetany, hemorrhage, cardiac
collapse
 True level of free Ca: ionized Ca level
Trousseau’s Sign
2. Hypercalcemia

Etiology and RF: Major Causes

 Metastatic malignancy (Tumor Lysis Syndrome)
 Hyperparathyroidism
 Thiazide diuretic therapy

 Other Causes:
 Excessive intake of Ca supplements w/ vit. D, Ca
containing antacids
 Prolonged immobilization
 Metabolic acidosis
 Hypophosphatemia
 ↑ Calcium

↑ cell membrane potential threshold

cell membrane becomes refractory to depolarization

cell membrane becomes less excitable and requires

greater stimulus to produce response
Clinical Manifestations:
 GI- anorexia, N/V, abdominal distention &
constipation
 Neurologic Depression – weakness, fatigue,
depression, difficulty concentrating
 Osmotic diuresis
 ureteral or kidney stones
 ECG Changes: short QT interval, widened T wave

(cardiac depression  dysrhythmias & arrest)

D. Phosphate Imbalances
 Phosphate promotes strong and durables bones
 Phosphate is an integral part of ATP, ADP
 Phosphate plasma level is regulated by PTH
 Facilitates release of Hgb and maintenance of acid-base balance,
nervous system, and intermediary metabolism of CHO, CHON, and fats

1. Hypophosphatemia
Etiology and RF:
 Major loss/ long term lack of intake
 Other RF: periods of ↑ ed growth or tse. Repair and recovery from
malnourished states
 Prolonged/ excessive intake of antacids
 Administration of high levels of glucose via tube feeding/ IV line

(glucose cause the P to enter the cell for glucose phosphorylation)

 ↑ ed Na+, ↑ ed Ca, ↓ ed PaCO2 in resp. alkalosis
 Lead poisoning
 Burns
Clinical Manifestations:
 ↓ ed cardiac and respiratory fxn
 Muscle weakness
 Fatigue
 Brittle bones
 Confusion and Seizures

2. Hyperphosphatemia
Etiology and RF:
 Excessive intake of high- PO4 foods
 Excess vit. D
 Impaired colonic motility from ↑ ed absorption
 Hypoparathyroidism and Addison’s dse.
 Renal failure
 TLS
 Post menopausal state
Clinical Manifestations:

 ↑ ed PR
 Palpitations
 Restlessness
 Anorexia, N/V, tetany, hyperreflexia, dydrhymias

Food rich in PO4:

 Milk, ice cream, cheese, large amounts of meat and fish,
carbonated beverages
 E. Magnesium Imbalances
 Actions similar to K+
 Signs of imbalance similar to K+
 2nd most abundant intracellular cation
 Fxns: transmission & conduction of nerve impulses
– Contraction of Muscle
– Responsible for the transportation of Na+ & K+
across cell membrane
– Responsible for the synthesis & release of PTH
 increased Ca and Phosphorus= can ↓ Mg absorption
from intestines
 ↓ ed Mg can lead to hypokalemia and hypocalcemia
 Acts as an activator for many
intracellular enzyme system and plays a
role in both carbohydrate and CHON
metabolism
 1/3 CHON bound
 2/3 free Mg
 Predominantly found in bones and soft
tissues and eliminated by the kidney.
 Hypomagnesemia
 Common cause of refractory hypokalemia and
hypocalcemia
 ETIOLOGY AND RF:
– Critically ill
– Alcoholics
– Malabsorption syndromes
– GI losses
– Diuretic phase of renal failure
– Excess Ca and excess Na inhibits Mg
– Prolonged IV or TPN therapy w/ Mg replacement
– Hyperglycemia, osmotic diuresis
– Many medications
– Diuretics and antibiotics (aminoglycosides)
– Corticosteroids and digitalis – promotes uptake of Mg
– Estrogen
Clinical Manifestations:
 Myocardial irritability
 Anorexia, nausea, abdominal distention
 Psychological disorders
 Neuromuscular Manifestations- Chvostek’s sign,
Trousseau’s sign, tetany, convulsions, vasospasm
leading to stroke
 ECG changes – prolonged QT, widened QRS,
broadened T-waves
2. Hypermagnesemia

Etiology and RF:

 Renal insufficiency
 Excessive use of Mg- containing antacids
 Excessive use of Mg- containing laxatives
 Administration of K+ sparing diuretics
 Severe dhn from DKA
 ↓ ed synthesis of aldosterone
 Overuse of IV MgSO4

Clinical Manifestations:
 Decreased muscle activity
 Hypotension
 Severe muscle weakness, lethargy, drowsiness, loss of deep tendon
reflex, respiratory paralysis and loss of consciousness
 ECG – prolonged PR interval, widened QRS
ACID BASE BALANCE

Concept : Normal functions of body cells depend or the

regulation of Hydrogen ion (H+) concentration – the
determinant of serum pH (acidity/ alkalinity)

Acid-Base Balance – refers to the Hydrogen (H+) ion

concentration in the body.
Acid- a substance which when dissolved in H20 can
dissociate and increase the H+ ion concentration;
hydrogen ion donor.
Base – a substance which when dissolved in H20 can
dissociate and increase the Hydrogen ion (OH)
concentration and the therefore neutralizes the
hydrogen ions; hydrogen ion acceptor
pH – used to express the degree of acidity or alkalinity of a
solution; normal serum pHs 7.35 -7.45

Normal concentrations of H+ in the body fluids: 0.00004

mEq/L

Functions of H+
 Necessary for proper cellular function
 Efficient functioning of every system
 Binding of O2 with hemoglobin
 Acts as powerful chemical adjutator with body fluids
 Determines the alkalinity and acidity of solution
Regulation of Acid-Base Balance

1. Modulation of serum pH blood buffer system

Buffer System – consist of weak acid and salt of base

which act together to neutralize either acid or bases;
body line of defense against acid-base imbalance.

Bicarbonate Buffer System:

-Most important buffer system in the body (ECF)
-Comprises 1/12 of the buffer system
 NaH CO3(Bicarbonate)
– Weak base
– Regulated by the kidneys
H2CO3 (Carbonic Acid)
– A weak acid
– Regulated by the lungs through respiration
 In order to maintain the ph at a normal level (7.35-7.45 or
an average of 7.4) the ration of bicarbonate to carbonic
acid must be 20:1.
 The pH of buffered solutions tend to remain fairly stable
despite the addition of strong acids or bases because the
buffer system converts them to weaker forms.
2.Regulation of volatile acid by the lungs

Volatile Acids- acids that can be converted to gases.

Carbon dioxide – potential acid; continuously produces by
body cells as an end product of complete oxidative
metabolism of nutrients for energy.
– 99.9 % of carbonic acid dissociates into CO2 to H2o. therefore by
increasing or decreasing respiration, Co2 can be conserved or lost;
and carbonic acid concentration is affected.
 The pH of the blood stimulates the respiration center so
that respiration are increased in alkalosis or decrease in
acidosis
 hypoventilation – hypercapnea (increased CO2)
 hyperventilation –hypocapnea (decrease CO2)
3.Regulation of fixed Acids and Bicarbonate by the Kidneys

The Kidneys regulate bicarbonate concentration by:

 Excreting excess acid/base
 Reabsorbing needed base

Urinary Buffer System- the kidney regulate serum pH by secreting

H+ into the urine and by regenerating HCO3 for reabsorption into
the blood; permits tubular fluid to accept large quantities of H+
while limiting how much the urinary pH decreases.

pH is the direct indication of acidity (increased H+ concentration )

or alkalinity (decreased H+ concentration)
 pCo2 is inversely proportional with pH
– HCO3 and pO2 is directly proportional with pH
– pO2 and H2Co3 is directly proportional
Normal Values of ABG ( arterial blood Gas) Analysis
pH = 7.35 to 7.45 mmHg
pCO2 = 34-45 mmHg
HCO3 = 24-26 mEq/L
pO2 = 90 -110 mmHg

In order to interpret ABG result, remember the following

 pCO2 = respiratory parameter

where: = acidosis
=alkalosis
 HCO3 = metabolic parameter

where: = acidosis
= alkalosis
IV Site Selection for ABG
 Interpretation of the Arterial Blood Gas
Overview
The pH is a measurement of the acidity or alkalinity of the blood. It is inversely
proportional to the number of hydrogen ions (H+) in the blood. The more H+ present,
the lower the pH will be.
Likewise, the fewer H+ present, the higher the pH will be. The pH of a solution is
measured on a scale from 1 (very acidic) to 14 (very alkalotic). A liquid with a pH of 7,
such as water, is neutral (neither acidic nor alkalotic).

The normal blood pH range is 7.35 to 7.45. In order for normal metabolism to take
place, the body must maintain this narrow range at all times. When the pH is below
7.35, the blood is said to be acidic. Changes in body system functions that occur in an
acidic state include a decrease in the force of cardiac contractions, a decrease in the
vascular response to catecholamines, and a diminished response to the effects and
actions of certain medications.

When the pH is above 7.45, the blood is said to be alkalotic. An alkalotic state
interferes with tissue oxygenation and normal neurological and muscular functioning.

Significant changes in the blood pH above 7.8 or below 6.8 will interfere with cellular
functioning, and if uncorrected, will lead to death.
Components of the Arterial Blood Gas

pH: Measurement of acidity or alkalinity, based on the hydrogen

(H+) ions present.
The normal range is 7.35 to 7.45

PaO2: The partial pressure of oxygen that is dissolved in arterial

blood.
The normal range is 80 to 100 mm Hg.

SaO2: The arterial oxygen saturation.

The normal range is 95% to 100%.

PaCO2: The amount of carbon dioxide dissolved in arterial blood.

The normal range is 35 to 45 mm Hg.

HCO3: The calculated value of the amount of bicarbonate in the

bloodstream.
The normal range is 22 to 26 mEq/liter
 Step One
Assess the pH to determine if the
blood is within normal range,
alkalotic or acidotic. If it is above
7.45, the blood is alkalotic. If it is
below 7.35, the blood is acidotic.
 Step Two
If the blood is alkalotic or acidotic, we now need
to determine if it is caused primarily by a
respiratory or metabolic problem. To do this,
assess the PaCO2 level. Remember that with
a respiratory problem, as the pH decreases
below 7.35, the PaCO2 should rise. If the pH
rises above 7.45, the PaCO2 should fall.
Compare the pH and the PaCO2 values. If pH
and PaCO2 are indeed moving in opposite
directions, then the problem is primarily
respiratory in nature.
 Step Three
Finally, assess the HCO3 value. Recall that with
a metabolic problem, normally as the pH
increases, the HCO3 should also increase.
Likewise, as the pH decreases, so should the
HCO3. Compare the two values. If they are
moving in the same direction, then the
problem is primarily metabolic in nature. The
following chart summarizes the relationships
between pH, PaCO2 and HCO3.
 pH PaCO2 HCO3
 Respiratory Acidosis ↓ ↑ normal
 Respiratory Alkalosis ↑ ↓ normal
 Metabolic Acidosis ↓ normal ↓
 Metabolic Alkalosis ↑ normal ↑
Jane Doe is a 45-year-old female admitted to the nursing unit
with a severe asthma attack. She has been experiencing
increasing shortness of breath since admission three hours
ago.
Her arterial blood gas result is as follows:
 pH 7.22
 PaCO2 55
 HCO3 25

 Follow the steps:

1. Assess the pH. It is low (normal 7.35-7.45);therefore, we have
acidosis.
2. Assess the PaCO2. It is high (normal 35-45) and in the
opposite direction of the pH.
3. Assess the HCO3. It has remained within the normal range
(22-26).
 pH PCO2 HCO3
Respiratory Acidosis ↓ ↑ Normal

 Refer to the chart. Acidosis is present

(decreased pH) with the PaCO3 being
increased, reflecting a primary respiratory
problem. For this patient, we need to improve
the ventilation status by providing oxygen
therapy, mechanical ventilation, pulmonary
toilet or by administering bronchodilators.
 John Doe is a 55-year-old male admitted to your
nursing unit with a recurring bowel obstruction. He
has been experiencing intractable vomiting for the
last several hours despite the use of antiemetics.
Here is his arterial blood gas result:
 pH 7.50
 PaCO2 42
 HCO3 33

 Follow the three steps again:

7. Assess the pH. It is high (normal 7.35-7.45)

2. Assess the PaCO2.

3. Assess the HCO3.

 pH PCO2 HCO3
Metabolic Alkalosis ↑ normal ↑

 Again, look at the chart. Alkalosis is

present (increased pH) with the HCO3
increased, reflecting a primary
metabolic problem. Treatment of this
patient might include the administration
of I.V. fluids and measures to reduce
the excess base.
Compensation
 When a patient develops an acid-base imbalance,
the body attempts to compensate. Remember that
the lungs and the kidneys are the primary buffer
response systems in the body. The body tries to
overcome either a respiratory or metabolic
dysfunction in an attempt to return the Ph into the
normal range.

A patient can be uncompensated, partially

compensated, or fully compensated. When an acid-
base disorder is either uncompensated or partially
compensated, the pH remains outside the normal
range. In fully compensated states, the pH has
returned to within the normal range, although the
other values may still be abnormal. Be aware that
neither system has the ability to overcompensate.
Partial compensation:

 1. Assess the pH.

 2. Assess the PaCO2. In an uncompensated state, we have already seen

that the pH and PaCO2 move in opposite directions when indicating that the
primary problem is respiratory. But what if the pH and PaCO2 are moving in
the same direction? We would then conclude that the primary problem was
metabolic. In this case, the decreasing PaCO2 indicates that the lungs,
acting as a buffer response, are attempting to correct the pH back into its
normal range by decreasing the PaCO2. If evidence of compensation is
present, but the pH has not yet been corrected to within its normal range,
this would be described as a metabolic disorder with a partial respiratory
compensation.

 3. Assess the HCO3. In our original uncompensated examples, the pH and

HCO3 move in the same direction, indicating that the primary problem was
metabolic. But what if our results show the pH and HCO3 moving in
opposite directions? That is not what we would expect to see. We would
conclude that the primary acid-base disorder is respiratory, and that the
kidneys, again acting as a buffer response system, are compensating by
retaining HCO3, ultimately attempting to return the pH back towards the
normal range.
Partially Compensated States
pH PaCO2 HCO3
Respiratory Acidosis ↓ ↑ ↑
Respiratory Alkalosis ↑ ↓ ↓
Metabolic Acidosis ↓ ↓ ↓
Metabolic Alkalosis ↑ ↑ ↑

Fully Compensated States

pH PaCO2 HCO3

Respiratory Acidosis normal ↑ ↑

but <7.40
Respiratory Alkalosis normal ↓ ↓
but >7.40
Metabolic Acidosis normal ↓ ↓
but <7.40
Metabolic Alkalosis normal ↑ ↑
but >7.40
 John Doe is admitted to the hospital. He is a
kidney dialysis patient who has missed his
last two appointments at the dialysis center.
His arterial blood gas values are reported as
follows:

 pH 7.32
 PaCO2 32
 HCO3 - 18
 pH PaCO2 HCO3

Metabolic Acidosis ↓ ↓ ↓
1. Assess the pH. It is low (normal 7.35-7.45); therefore we have
acidosis.
2. Assess the PaCO2. It is low. Normally we would expect the pH and
PaCO2 to move in opposite directions, but this is not the case. Because
the pH and PaCO2 are moving in the same direction, it indicates that
the acid-base disorder is primarily metabolic. In this case, the lungs,
acting as the primary acid-base buffer, are now attempting to
compensate by “blowing off excessive C02”, and therefore increasing
the pH.
3. Assess the HCO3. It is low (normal 22-26). We would expect the pH
and the HCO3 to move in the same direction, confirming that the
primary problem is metabolic.

Because there is evidence of compensation (pH and PaCO2 moving in the

same direction) and because the pH remains below the normal range, we
would interpret this ABG result as a partially compensated metabolic acidosis.
Jane Doe is a patient with chronic COPD
being admitted for surgery. Her admission lab
work reveals an arterial blood gas with the
following values:

pH = 7.35
PaCO2 = 48
HCO3 = 28
 pH PaCO2 HCO3
Respiratory Acidosis normal ↑ ↑
but <7.40
1. Assess the pH. It is within the normal range, but on the low side
of neutral (<7.40).

2. Assess the PaCO2. It is high (normal 35-45). We would expect

the pH and PaCO2 to move in opposite directions if the primary
problem is respiratory.

3. Assess the HCO3. It is also high (22-26). Normally, the pH and

HCO3 should move in the same direction. Because they are
moving in opposite directions, it confirms that the primary acid-
base disorder is respiratory and that the kidneys are attempting
to compensate by retaining HCO3. Because the pH has returned
into the low normal range, we would interpret this ABG as a fully
compensated respiratory acidosis.